Should You Take Probiotics?


Probiotics are live bacteria and yeasts that can live in your body and help to keep you healthy. These healthful bacteria make vitamins, help to digest food, regulate inflammation, and help to limit the number of disease-causing microbes living in your body. Probiotics are found in live-culture fermented foods such as yogurt, kefir (a probiotic milk drink), buttermilk, kombucha (fermented tea), tempeh, miso and natto (fermented soybean products), kimchi, sauerkraut, some pickles, and some fermented cheeses. They are also found in over-the-counter pills that claim to contain live bacteria that will improve your health. However, many scientists have concerns about taking over-the-counter probiotic pills because:
• the healthful bacteria can mutate into bacteria that have harmful properties, and
• the bacteria in pills usually disappear from your intestines soon after you stop taking the pills.

You have more than 100 trillion bacteria living in your intestines. They can be:
• harmful bacteria that are not happy to eat the same foods that you eat, so they try to invade your intestinal cells and bloodstream which can make you sick, or
• healthful bacteria that do not try to invade the cells lining your intestines and eat the same foods that you eat. The healthful bacteria can help to prevent constipation, diarrhea, and irritable bowel syndrome, can lower high blood sugar, cholesterol and blood pressure and possibly even help to prevent and treat diabetes, arteriosclerosis and certain cancers. These “good” bacteria help to protect you from the “bad” bacteria by causing your intestinal cells to produce a layer of mucous that coats the cells lining your intestines, to help prevent the harmful bacteria from invading your intestinal cells and passing into your bloodstream.

Bacterial DNA Can Change in Your Body
Researchers at Washington University School of Medicine in St. Louis gave a large number of mice a probiotic strain of bacteria called “Escherichia coli Nissle 1917” that is sold over-the-counter to treat diarrhea and promote health (Cell Host and Microbe, March 26, 2019). This strain of bacteria was isolated more than one hundred years ago from the stool of a World War I soldier who was one of the few soldiers not sickened during an epidemic of severe diarrheal disease that killed many of the other soldiers.

After just a few weeks, the healthful “E. coli Nissle 1917” bacteria in some of the mice changed their DNA so that instead of making protective mucus to coat the intestines, the bacteria were able to eat through the protective coating on the intestines and then invade intestinal cells, the way the harmful bacteria do. This is what appears to happen when humans develop irritable bowel syndrome.

Interestingly, the change of healthful bacteria to harmful bacteria was influenced by what the mice ate. First, researchers gave groups of mice the “E. coli Nissle 1917” probiotic, and then put them on different diets:
• a regular mouse diet,
• high-fiber pellets that otherwise contained the same foods as the regular mouse diet,
• high-fat, high-sugar, low-fiber pellets (to mimic humans’ typical Western diet), and
• high-fat, high-sugar pellets plus fiber.

After five weeks, researchers checked the DNA of the mice’s intestinal bacteria and found no change in the DNA of the “E. Coli Nissle 1917” bacteria in the mice given a healthful high-fiber diet, but a significant change in the DNA of the bacteria of the mice on the high-sugar, high-fat, low-fiber diet. The high-sugar, high-fat diet was associated with an intestinal change from the healthful probiotic bacteria into harmful bacteria.
• On the high-fiber healthful diet, the probiotic bacteria retained their healthful function.
• On the high-sugar diet, the probiotic bacteria adjusted to feed on the different sugars.
• The high-sugar diet converted the healthful bacteria that originally did not enter the intestinal cells and produced mucous to protect the cells lining the intestines into harmful bacteria that entered and ate the cells lining the intestines.
• When exposed to antibiotics, the probiotic bacteria rapidly developed a resistance to the antibiotics.

Should You Take Probiotics?
A review of 45 scientifically-controlled studies published over the last 27 years (European Journal of Clinical Nutrition, March 26, 2018) shows that in healthy people, the use of probiotic supplements can:
• lead to an increase in these healthful bacteria growing in your colon
• reduce belly discomfort caused by irregular bowel movements and constipation
• improve some immune system responses, stool consistency, bowel movements, and the concentration of healthful bacteria in the colon and vagina
However, these benefits are only temporary as the bacteria in the probiotics stop growing in the colon or vagina soon after a person stops taking the probiotic product. Permanent changes to a more healthful colony of gut bacteria appear to occur only when people make permanent changes to their diets. The probiotic supplements studied in this review included live healthful bacteria packaged in capsules, powders and liquids or those found in live-culture fermented foods such as yogurt or kefir.

Probiotics May Help to Prevent Overgrowth of Harmful Bacteria When You Take Antibiotics
Antibiotics prescribed by your doctor can knock off your good bacteria as well as the bad ones. A review of 39 studies shows that taking probiotics (Saccharomyces, Lactobacilli, Bifidobacteria, and Streptococci) at the same time you take antibiotics can reduce the incidence of diarrhea and super-infections with a harmful bacteria called Clostridia difficile (JAMA, 2018;320(5):499-500).

However, taking probiotic bacteria after you take antibiotics to treat an infection can prevent other healthful bacteria from regrowing in your intestines, to significantly increase your chances of developing allergies and also your increase risk for inflammation that is caused by harmful colon bacteria that try to invade your colon cells (Cell, 2018 Sep 6;174(6):1388-1405.e21). Those who did not take probiotics after taking antibiotics had their healthful intestinal bacteria return to normal much more quickly. The message from this study is that after taking antibiotics that have destroyed your normal bacteria in your intestines, taking probiotics may prevent your usual intestinal bacteria from returning to normal.

Probiotics are Worthless with an Unhealthful Lifestyle
The study from Washington University suggests how quickly an unhealthful diet may cause changes in your gut bacteria. Since healthful bacteria in your colon eat the same food that you do, the best way to grow healthful bacteria is to eat a diet with lots of the foods that encourage the growth of healthful bacteria. Soluble fiber in plants now appears to be the most effective way to grow healthful bacteria in your colon, prevent disease and prolong your life. See The More Vegetables, The Better. The number of harmful colon bacteria increases with certain harmful lifestyle factors such as:
• not eating lots of vegetables and fruits
• eating a lot of pro-inflammatory foods (such as meats, foods with added sugars, sugared drinks and other refined carbohydrates)
• drinking alcohol
• smoking
• not exercising
• being overweight, particularly storing fat in your liver

My Recommendations
Since we have no way to know what is actually in probiotic capsules, drinks or other probiotic products, I recommend that you concentrate on the foods that are known to help you grow a colony of healthful colon bacteria — fruits, vegetables, whole grains, beans, nuts and other seeds — and work to change any of the harmful lifestyle factors listed above that apply to you. You may benefit from taking a probiotic such as live-culture yogurt any time you need to take a prescription for antibiotics to treat an infection.

Bad Colon Bacteria May Cause Heart Attacks


You have more than 100 trillion bacteria living in your colon, with some types that are helpful and other types that are harmful. With aging, the ratio of good to bad types of bacteria appears to change, increasing the amounts of harmful bacteria and reducing the amounts of healthful bacteria. Harmful colon bacteria have been shown to increase risk for many diseases by producing chemicals that cause inflammation. A strong new study shows that with aging, there is an increase in the types of harmful colon bacteria that produce amines, specifically TMAO (trimethylamine oxide), that damage arteries to increase risk for heart attacks, strokes and cell damage throughout your body (J Physiol, Feb 4, 2019).

The Study
With aging, mice (like humans) suffer progressive changes in their arteries that can lead to heart attacks, strokes and cancers. Older mice, but not younger mice, suffer damage to the inner linings of their arteries and arterial stiffness so their arteries cannot widen to increase blood flow when needed as healthy blood vessels do. Arterial stiffness is associated with increased risk for heart attacks, strokes, and cell damage. Scientists can measure the factors that increase risk for arterial damage with aging.

In this study the researchers looked for the harmful pro-inflammatory, tissue-damaging free radicals. They were also able to measure factors that reduce arterial damage such as healthful antioxidants and nitric oxide. Groups of young and old mice were given poorly-absorbed, broad-spectrum antibiotics to kill large amounts of the bacteria that live in their colons. They used genetic sequencing to determine the types of bacteria in the mice’s stools and found that the antibiotics reduced the number of harmful colon bacteria in both young and old mice. After 3-4 weeks, the researchers found no change in the arteries of the young mice, but the old mice had improvements in their arterial stiffness and in the inner linings of their arteries. Both the young mice and the old mice had lower levels of the harmful TMAO, and higher levels of healthful antioxidants.

Note that giving antibiotics to kill colon bacteria was an experimental technique used on mice to mimic changes that occur with aging in humans. The researchers are not suggesting that antibiotics should be given to alter gut bacteria in humans.

Other Studies on Colon Bacteria
Some types of colon bacteria affect risk for many conditions and diseases (JAMA, May 14, 2018), such as:
• Obesity – Colon bacteria break down unabsorbed foods to determine what percentage of the calories from food you absorb (Nature, June 9, 2016;534:213-217). Giving baby mice penicillin, in doses similar to what farmers give livestock, changed their colon bacteria into the types that made them fat and caused them to develop 15 percent more body fat than mice not given antibiotics, and they remained fat into later life (Cell, August 14, 2014;158(4):705-721).
• Type 2 Diabetes – Healthful colon bacteria turn soluble fiber into short chain fatty acids (SCFAs) that reduce inflammation to help prevent and treat diabetes (Front Microbiol, Feb 17, 2016;7:185).
• Heart attacks – Harmful colon bacteria cause inflammation that damages arteries (Am J Clin Nutr, Dec, 2005;82(6):1185-94).
• High Cholesterol – Harmful colon bacteria decrease the rate that your body makes bile to increase blood levels of the harmful LDL cholesterol that increases risk for heart attacks (Cell Metab, 2013;17(2):225-235).
• High Blood Pressure – Healthful colon bacteria increase production of SCFAs that lower high blood pressure (Proc Natl Acad Sci USA, 2013;110(11):4410-4415).
• Inflammatory bowel diseases – SCFAs produced by healthful gut bacteria reduce symptoms of ulcerative colitis and Crohn’s disease (Inflam Bowel Dis, Mar 2003;9(2):116-21).

How Colon Bacteria Affect Your Health
Harmful colon bacteria try to enter your colon cells which causes your immune system to produce cells and chemicals that attack and kill bacteria and other invading germs. When your immune system is turned on all the time, these same cells can attack and destroy your own cells to increase risk for arteriosclerosis, diabetes, obesity, heart attacks, cancers, dementia and other diseases. Healthful colon bacteria convert soluble fiber into SCFAs that protect you from disease by decreasing inflammation that can damage every cell in your body, and by lowering high cholesterol and high blood pressure.

My Recommendations
Your current diet determines which bacteria live in your gut. Even if your colon is full of harmful bacteria, you can change your colon bacteria by switching to an anti-inflammatory, high-fiber diet that includes a wide variety of vegetables, whole grains, beans, nuts and other seeds. A healthful diet, together with weight control, a regular exercise program, and avoidance of alcohol and smoke, will help to protect you from the many diseases that are linked to the typical Western diet and lifestyle.

Intense Exercisers Have More Plaques but Fewer Heart Attacks


The MARC-2 study followed 291 older men for 6.3 years with a test called Coronary Artery Calcification (CAC), and found that the amount of calcium in the arteries leading to the heart increased most in men who exercised at the highest intensity, even more than those who exercised the most (Circulation, January 4, 2023). The authors said this showed that intense exercise increases the amount of plaques in arteries, which may be true. However, they would then have to explain why intense exercisers are far less likely to suffer heart attacks than non-exercisers (JAMA Cardiol, 2019;4(2):174-181). Exercise is prescribed both to treat and to prevent heart attacks (Front Cardiovasc Med, Feb 3, 2021;8:753672).
• CAC measures only the size of plaques. It does not measure obstruction of blood flow to the heart. Furthermore, as plaques form, the involved arteries usually widen to accommodate the plaques (JAMA Cardiol, October 27, 2021).
• Intense exercise increases the amount of calcium in plaques (Circulation, January 4, 2023). Calcium in plaques stabilizes them to help prevent plaques from breaking off, which is the cause of most heart attacks.

Heart Attacks Are Caused by Plaques Breaking Off from Coronary Arteries
Heart attacks have little to do with arteries being narrowed by plaques. A heart attack is caused by a sudden immediate complete blockage of blood flow to the heart muscle itself. First a plaque breaks off from the inner lining of an artery leading to the heart. This is followed by bleeding and clotting. Then the clot extends to block all flow of blood through that artery to deprive the heart muscle completely of oxygen, so that part of the heart muscle dies.

An X-ray test called Coronary Artery Calcification Score or Calcium Artery Score (CAC) is used to measure the size of plaques in the arteries leading to the heart. That test can also tell whether the plaques are very stable, or are unstable and more likely to break off to cause a heart attack. A stable plaque is called “hard; ” it is not full of fat and has a thick calcium periphery to keep the plaque in place. An unstable plaque is called “soft;” it is full of fat and has irregular calcium borders that may not hold the plaque in place.

Plaques are Formed from an Unhealthful Diet
Exercise does not prevent plaques from forming. A diet that is high in the pro-inflammatory foods (sweets, refined grains, sugared drinks, red meat, processed meats, fried foods, alcohol) is associated with increased risk for forming plaques (Journal of the American College of Cardiology, July 2017;70(4)). A heart-attack-preventing diet that is high in vegetables, fruits, whole grains, beans, seeds and nuts will reduce your chances of growing larger plaques. You also should avoid being overweight or smoking.

Why Exercisers May Have Higher Calcium Scores
Competitive older endurance athletes can have more plaques in their arteries than non-exercisers, and intense exercise may increase plaque formation. However, the endurance athletes are likely to have the type of plaques that are far less likely to break off to cause heart attacks (Circulation, April 27, 2017;136:138-148; May 2, 2017;136:126-137). Plaques form in arteries from an unhealthful diet and perhaps faulty genes. Exercise does not prevent plaques from forming, and a pro-inflammatory diet increases plaque formation regardless of exercise. Exercise stabilizes plaques so that they are less likely to break off to cause heart attacks. Since exercise burns lots of extra calories, exercisers may eat more food, and if they choose to add more pro-inflammatory foods, they can expect to build up more plaques.

My Recommendations
A high Coronary Artery Calcium test (CAC) has been shown to be associated with increased risk for a heart attack, but regular exercisers may have higher CAC test results because they have more calcium in their plaques. These more stable plaques are less likely to break off and cause a heart attack. Since exercise stabilizes plaques to help keep them from breaking off from arteries, exercise should be part of your heart-attack-prevention program. You should check with your doctor about exercising if you have evidence of heart disease caused by a faulty diet: high blood cholesterol, triglycerides, sugar or CRP, high blood pressure, an abnormal EKG, or chest pain particularly with exercise.

Journal References on Coronary Artery Calcium Tests (CAC)
• CAC measures amount of plaques in a person’s arteries (J Am Coll Cardiol, 1998;31:126–33).
• CAC is an excellent predictor of likelihood to suffer a heart attack in both younger and older men (Am J Epidemiol, 2005;162:421–9; Eur Heart J, 2008;29:2782–91; J Am Coll Cardiol, 2018 Jul 24; 72(4): 434–447).
• CAC measures the size of plaques in a person’s heart arteries (J Am Coll Cardiol, 1998;31:126–33).
• Physical activity increases CAC progression (Heart, Nov 2021;107(21):1710-1716).
• Increased CAC associated with increased heart attack risk (Am J Cardiol, 2017 May 15;119(10):1584-1589).
• Life-long middle-aged male endurance athletes have high CAC scores (European Heart J, July 21, 2021;42(28):2737–2744)

Five billion people unprotected from trans fat leading to heart disease


Five billion people globally remain unprotected from harmful trans fat, a new status report from WHO has found, increasing their risk of heart disease and death.

Since WHO first called for the global elimination of industrially produced trans fat in 2018 – with an elimination target set for 2023 – population coverage of best-practice policies has increased almost six-fold. Forty-three countries have now implemented best-practice policies for tackling trans fat in food, with 2.8 billion people protected globally.

Despite substantial progress, however, this still leaves 5 billion worldwide at risk from trans fat’s devastating health impacts with the global goal for its total elimination in 2023 remaining unattainable at this time.

Industrially produced trans fat (also called industrially produced trans-fatty acids) is commonly found in packaged foods, baked goods, cooking oils and spreads. Trans fat intake is responsible for up to 500 000 premature deaths from coronary heart disease each year around the world.

“Trans fat has no known benefit, and huge health risks that incur huge costs for health systems,” said WHO Director-General, Dr Tedros Adhanom Ghebreyesus. “By contrast, eliminating trans fat is cost effective and has enormous benefits for health. Put simply, trans fat is a toxic chemical that kills, and should have no place in food. It’s time to get rid of it once and for all.”

Currently, 9 of the 16 countries with the highest estimated proportion of coronary heart disease deaths caused by trans fat intake do not have a best-practice policy. They are Australia, Azerbaijan, Bhutan, Ecuador, Egypt, Iran (Islamic Republic of), Nepal, Pakistan and Republic of Korea.

Best-practices in trans fat elimination policies follow specific criteria established by WHO and limit industrially produced trans fat in all settings. There are two best-practice policy alternatives: 1) mandatory national limit of 2 grams of industrially produced trans fat per 100 grams of total fat in all foods; and 2) mandatory national ban on the production or use of partially hydrogenated oils (a major source of trans fat) as an ingredient in all foods.

“Progress in eliminating trans fat is at risk of stalling, and trans fat continues to kill people,” said Dr Tom Frieden, President and CEO of Resolve to Save Lives. “Every government can stop these preventable deaths by passing a best-practice policy now. The days of trans fat killing people are numbered – but governments must act to end this preventable tragedy.”

While most trans fat elimination policies to date have been implemented in higher-income countries (largely in the Americas and in Europe), an increasing number of middle-income countries are implementing or adopting these policies, including Argentina, Bangladesh, India, Paraguay, Philippines and Ukraine. Best-practice policies are also being considered in Mexico, Nigeria and Sri Lanka in 2023. If passed, Nigeria would be the second and most populous country in Africa to put a best-practice trans fat elimination policy in place. No low-income countries have yet adopted a best-practice policy to eliminate trans fat.

In 2023, WHO recommends that countries focus on these four areas: adopting best-practice policy, monitoring and surveillance, healthy oil replacements and advocacy. WHO guidance has been developed to help countries make rapid advances in these areas.

WHO also encourages food manufacturers to eliminate industrially produced trans fat from their products, aligning to the commitment made by the International Food and Beverage Alliance (IFBA). Major suppliers of oils and fats are asked to remove industrially produced trans fat from the products sold to food manufacturers globally.

The report, called Countdown to 2023 WHO Report on global trans fat elimination 2022, is an annual status report published by WHO in collaboration with Resolve to Save Lives, to track progress towards the goal of trans fat elimination in 2023.

Source: WHO

RSV Is Spreading: What We Know about This Common and Surprisingly Dangerous Virus


RSV Is Spreading: What We Know about This Common and Surprisingly Dangerous Virus

Moderna announced this week that its respiratory syncytial virus (RSV) vaccine is 84 percent effective at preventing lower respiratory disease in older adults. Scientific American answered common questions about the virus, its treatments and previously tested vaccines in this story from last November.

As flu season picks up and experts weigh concerns about another possible COVID surge, children’s hospitals are already filling with patients with another viral threat: respiratory syncytial virus, or RSV. Even though many people haven’t heard of RSV, pretty much everyone has had it, probably multiple times, says Anthony Flores, chief of pediatric infectious diseases at the University of Texas Health Science Center at Houston and a physician at Children’s Memorial Hermann Hospital. RSV is the leading cause of bronchiolitis—inflammation of the lung’s small airways—in infants, and the virus is so common that nearly all children have encountered it by their second birthday.

“It’s that ubiquitous,” Flores says. “Even adults are exposed to it repeatedly over time, so we develop some immunity to it.” In healthy adults and children, though, RSV typically presents as a common cold, with symptoms similar to those caused by other “common cold” viruses, such as rhinovirus, adenovirus and a couple of common coronaviruses. But that doesn’t mean it’s harmless. RSV costs the U.S. more than $1 billion each year in health care costs and lost productivity, and it can be particularly dangerous for newborn babies and adults older than age 65.

“As we have come to learn, particularly gradually over the last 15 years, this is a virus that annually produces probably about as much illness in adults as does influenza,” says William Schaffner, a professor of medicine at Vanderbilt University Medical Center and medical director of the National Foundation for Infectious Diseases. That’s because our immune system ages along with us. “As we get older, our immune system doesn’t work as well,” Flores says.

The good news is that RSV vaccines are on the way. In fact, Pfizer just announced this week that its maternal RSV vaccine—given during pregnancy so that antibodies are transferred through the placenta to the fetus—was 82 percent effective at preventing severe RSV in babies through three months old. But until the U.S. Food and Drug Administration approves a vaccine, RSV will be one of the unavoidable viruses people encounter each year.

What is RSV, and what are its symptoms?

RSV is an RNA virus made up of 11 proteins, similar to influenza A, another RNA virus whose genes encode the same number of proteins. It infects the nose, throat, lungs and the breathing passages of the upper and lower respiratory system, according to the National Foundation for Infectious Diseases. As the body sends immune cells to virus-infected cells to fight the disease, it causes inflammation in the airways.

Symptoms include a runny nose, reduced appetite, coughing, sneezing, wheezing and sometimes a mild fever—although fever is more common in young infants and older adults. Symptoms show up about four to six days after infection and take one to two weeks to resolve.

How is RSV transmitted?

RSV spreads primarily through respiratory droplets from coughing, sneezing and kissing (transmission by airborne droplets, or aerosols, has not yet been shown). But the virus can also survive for several hours on hard surfaces, including tables and crib rails. Such “fomites” are a more common mode of transmission for RSV than they are for COVID. People infected with RSV are typically contagious for about three to eight days, even if they don’t have many symptoms.

The basic reproduction number, or R0, for RSV is estimated to be around 3, which means a single infection of RSV will lead, on average, to three other infections.

How severe is an RSV infection?

For the average person, RSV is little more than a nuisance, Flores says. “For most of us—children over the age of two and healthy adults—it’s just like a common cold,” Flores says. “It may give us a little bit of a cough and runny nose, maybe a mild fever, but we usually get over it pretty quickly.”

But infants under six months old, and especially those under two months old, have a harder time with RSV. “That’s where we see our highest hospitalization rates [in children]—maybe three or four times higher in that age group than in others,” Flores says. The reason is basic physics. “It has everything to do with the size of their airways,” he says. Their airways simply aren’t wide enough yet to allow airflow with all the inflammation caused by the immune system’s response to the virus.

Even then, only about 1 to 2 percent of children under six months with RSV need hospitalization (usually for a couple of days), and death is rare. An estimated 58,000 U.S. children are hospitalized with RSV each year, and the virus kills about 100 to 500 U.S. children under five each year. (Since the pandemic began, COVID has killed more than 560 children under five, according to the U.S. Centers for Disease Control and Prevention.) Premature babies and those with underlying heart and lung conditions have the greatest likelihood of complications and hospitalization. Premature infants’ lungs tend to be underdeveloped and even less capable of handling the inflammation caused by the virus. In fact, children who meet strict criteria for being at highest risk are recommended to receive the preventive antibody medication palivizumab as an injection into the thigh muscle once a month when RSV is circulating.

Adults older than age 65 are also at risk of severe RSV, although public health officials have only begun to recognize the threat to older adults in the past decade. Every year an estimated 177,000 older adults are hospitalized with RSV, and about 14,000 die from it. For comparison, influenza kills anywhere from 21,000 to more than 44,000 adults older than 65 each year.

Another population at higher risk for complications from RSV are people who are immunocompromised, whether because they have an underlying condition that weakens their immune system or because they take a medication that suppresses it. Those who have had organ transplants, for example, take medications that dampen their body’s immune response to avoid rejection of the new organ. And many of the drugs used to treat autoimmune conditions also weaken the immune system.

Why are cases surging now?

Historically, RSV season was so reliable that children’s hospitals planned staffing around it. It typically ran from about November through April, with the biggest peaks in January and February, depending on local conditions. But the pandemic changed everything. With many people staying home, social distancing, washing hands and wearing masks for most of 2020 and into 2021, RSV—like influenza—never really arrived, and its seasonality has been out of whack ever since.

“All of a sudden, last summer, we had this huge surge of RSV,” Flores says. “At it first baffled everybody, but then it kind of epidemiologically made sense.” Normally, most kids encounter RSV some time in their first year and a half of life and develop some immunity as they recover. The immunity doesn’t last very long, but enough of it lingers that subsequent infections aren’t as severe. But thanks to the social distancing and masking, a whole birth cohort of kids had never been exposed to RSV before. So as society began opening back up in the summer of 2021, all of them were exposed at once, and RSV roared back like it was Christmas in July.

“We tended to see more severe reactions, so we saw more hospitalizations, and I think it’s because we had a larger pool of kids who had never been exposed to RSV in the past,” Flores says. That summer surge eventually settled down, but fast-forward to 2022, and although it’s later in the year, something similar is happening.

On one hand, current pediatric hospitalizations aren’t much higher at Flores’s hospital and many other hospitals than they would be during a typical RSV peak in midwinter. But the problem is that it’s not midwinter yet. With flu cases rising, pediatricians and public health experts are asking themselves the same question: “Are we going to see another surge with COVID later this year and then see a ‘tripledemic’?” Flores says. “That’s the big worry.” Flores doesn’t think a triple surge would necessarily cause more deaths, but it would place a significant burden on the health care system that many places aren’t prepared to weather.

Is there a vaccine for RSV?

There is no approved RSV vaccine yet, but there likely will be soon. Scientists have been working on such a vaccine for half a century, but a disastrous trial in the 1960s resulted in the deaths of two toddlers who caught RSV after receiving the vaccine. It turned out the disease was more severe in those who were vaccinated, and until that mystery was resolved, not much progress occurred. Fortunately, one of the same scientists whose team determined the spike-protein mRNA code for the COVID vaccines, Jason McLellan of the University of Texas, solved the RSV vaccine problem with virologist Barney Graham, then at the National Institutes of Health, about decade ago. Now that work is coming to fruition.

Several pharmaceutical companies began vaccine trials with McLellan’s protein in 2017, and the first successful phase III (late-stage) results came this year. Against severe disease, Pfizer’s vaccine was 86 percent effective and GSK’s was more than 94 percent effective in adults 60 and older.* Between those vaccines and Pfizer’s recent maternal RSV vaccine news, Graham, who is now retired from the NIH, expects to see at least one RSV vaccine approved by the end of 2023, if not sooner.

How is RSV treated?

There is no medication to treat RSV, so the treatment is primarily supportive care for symptoms such as fever and congestion. Those who have trouble breathing may receive a breathing tube or supplemental oxygen through a mask or nose tube. The American Academy of Pediatrics used to recommend steroids for infants, but the data are conflicting on how well they help, so that’s no longer a standard recommendation, Flores says.

There are a couple of reasons therapeutics don’t exist for RSV. First, it’s very difficult to develop effective drugs for respiratory virus infections. Most of the four antivirals available for flu, for example, are fairly new and have limited effectiveness unless given early after infection. Second, so few children die from RSV that therapeutics weren’t as high a priority as developing drugs for other conditions. The recent understanding of how many adults die from RSV and advances in monoclonal antibodies, however, have boosted the pipeline for new RSV treatments.

The drug furthest along is nirsevimab, which was 75 percent effective in healthy infants in a phase III trial and has been shown to be safe in premature infants as well. FDA approval could come late this year or next.

What should someone do if they think they or a family member has RSV?

Chances are, you won’t know if you have RSV because it will feel like any other cold. You should do “all those things we’ve learned in the pandemic” when you’re sick, Flores says. That means wearing a mask, practicing good hand hygiene, covering your mouth when you sneeze or cough and, for those able to do so, working from home. Many people won’t or can’t stay home from school or work with just a cold, though, so wearing a mask can at least protect others around you while you’re sick, especially those at higher risk for complications. If there’s anything we learned from the way flu and RSV basically disappeared in 2020, Flores says, it’s that masking obviously works. 

When should someone with RSV go to the hospital?

As with any other respiratory illness, the biggest sign that one should seek medical attention, regardless of age, is having difficulty breathing, Flores says. In addition, parents should take an infant under six months to the doctor or hospital if the child can’t lie down without breathing difficulty, if they’re sleepier than usual or if they’re difficult to rouse from sleep.

What can one do to protect vulnerable people from RSV?

Infants and young children who were born premature or who have weakened immune systems, chronic lung disease, congenital heart disease or a neuromuscular disorder may qualify to receive the drug palivizumab. Palivizumab is very expensive and in limited supply, so it’s reserved for those at highest risk, who will receive the most benefit from it. When the RSV season was more predictable, at-risk infants would begin receiving palivizumab in late fall, but when RSV’s seasonality shifted in 2021, state public health authorities convened to ensure the drug would become available when cases began rising.

For others at risk, including infants without underlying conditions, older adults and immunocompromised individuals, the same protections they take against COVID are also effective against RSV, as the low rates of RSV in 2020 showed. “When we see these surges like this, [vulnerable people are] absolutely instructed to be more careful,” Flores says. That means not having sick family members visit, washing hands regularly and wearing a mask outside the home to prevent not only COVID but also exposure to all the other seasonal respiratory viruses, including flu and RSV. And of course, Flores says, everyone eligible for a flu vaccine and COVID vaccine should ensure they’re vaccinated and boosted to reduce the risk of developing multiple infections at the same time.

Will Rezafungin Data for Serious Candida Infections Sway FDA Panel?


Agency reviewers highlight limited clinical trial data, neurotoxicity concerns

FDA ADCOMM rezafungin over a computer rendering of candida albicans fungus.

Ahead of an advisory committee meeting on Tuesdayopens in a new tab or window, FDA staff raised concerns over whether the potential benefits of weekly rezafungin injections for adults with candidemia and invasive candidiasis (IC) outweigh any potential risks, including neurotoxicity.

According to an agency briefing documentopens in a new tab or window for the Antimicrobial Drugs Advisory Committee, potential approval of the investigational, long-acting echinocandin for candidemia and IC caused by susceptible Candida species hinges on a single phase III non-inferiority study (ReSTORE), along with data from the dose-finding phase II STRIVE study.

“The key issues for consideration in the benefit-risk assessment of rezafungin include the presumed ability to meet an unmet need in the context of generally similar (to current treatment options) effects on survival, the ability to mitigate any identified risks such as neurotoxicity, and the acceptable tradeoffs between the benefits and risks to patients,” FDA staff wrote.

Candidemia and IC affect about 25,000 people per year in the U.S., according to the CDCopens in a new tab or window. The in-hospital all-cause mortality rate among people with candidemia is approximately 25%.

“There are three FDA-approved echinocandins, all of which are available only as intravenous (IV) formulations dosed once daily,” FDA staff noted. “Antifungal therapy is usually continued for 2 weeks after documented clearance of Candida spp. from the blood in the case of candidemia or following adequate source control and clinical response in IC.”

In the ReSTORE trial, which involved 187 subjects, rezafungin was found to be noninferior to caspofungin in the primary endpoint of all-cause mortality at 30 days in the modified intention-to-treat population, with rates of 23.7% in the rezafungin group versus 21.3% in the caspofungin group. Rezafungin was given as a 400-mg IV loading dose followed by weekly 200-mg IV doses for up to 4 weeks — the proposed clinical dose.

The safety dataset for rezafungin, submitted by sponsor Cidara Therapeutics, included 151 patients from ReSTORE who were given the proposed clinical dose and 81 patients from STRIVE given a higher dose (400 mg administered weekly).

In this dataset, tremor was observed in 2.6% of those receiving the proposed rezafungin dose compared with zero patients receiving caspofungin. Tremor was also reported in early nonhuman primate studies.

While the ReSTORE/STRIVE data “show a similar safety profile to the FDA-approved echinocandins, the size of the dataset limits the ability to identify rare adverse reactions that may be unique to rezafungin,” according to agency staff.

Although tremor has been reported to be an uncommon adverse reaction in the labeling of other echinocandins for candidemia/IC, the FDA noted that the trial data need further scrutiny.

“The review team’s assessment is that the Applicant has not provided sufficient data to support the position that rezafungin provides improved activity against Candida spp. with reduced susceptibility to FDA-approved echinocandins or provides improved tissue penetration,” the FDA wrote in its briefing document. “Overall, the review team finds that rezafungin is primarily distinguished from FDA-approved echinocandins by its extended half-life but welcomes the committee’s input on whether rezafungin may have additional benefits that would extend treatment options for patients with candidemia/IC to address an unmet need.”

All of the currently approved echinocandins, including caspofungin, anidulafungin, and micafungin, come with warnings for hypersensitivity reactions and hepatic adverse reactions in their labeling. Micafungin also has a warning for hematologic effects, renal effects, and infusion and injection site reactions, and anidulafungin has warnings related to risks associated with two of the inactive ingredients in its formulation.

“None of the echinocandins have warning statements related to neurotoxicity, and the only nervous system adverse reaction reported in >5% of patients in clinical trials was headache,” the FDA wrote.

Tremor was reported as an adverse reaction occurring in less than 5% of 68 pediatric patients in an open-label non-comparative study of anidulafungin, and in the pooled safety experience from 34 studies of caspofungin in adult and pediatric patients or volunteers (n=1,951).

During the planning of the ReSTORE trial, the FDA recommended safety measures to mitigate the risk of neurotoxicity, including the exclusion of patients “with a history of neuropathy, history of tremors, or [those] receiving neurotoxic medication; addition of safety assessments for neuropathy, ataxia, and tremor; and review of safety information by the data safety monitoring board.”

Currently, four classes of antifungals (echinocandins, azoles, amphotericin B formulations of polyenes, and flucytosine) have shown clinical effectiveness for the treatment of candidemia/IC. The Infectious Diseases Society of America recommends echinocandins as first-line therapy, except when infections affect the central nervous system, the eyes, or the urinary tract. The other antifungals are considered alternatives in the case of drug intolerance, drug-resistant pathogens, or as adjunctive therapy for refractory cases.

Diabetes Drug for Cats Now Approved in Humans Too


Oral SGLT2 inhibitor bexagliflozin indicated for adults with type 2 diabetes

FDA APPROVED bexagliflozin (Brenzavvy) over a photo of a glucose meter and other items related to diabetes.

The first oral SGLT2 inhibitor approved by the FDA for treating diabetes in catsopens in a new tab or window is now approved for humans with the disease, drugmaker opens in a new tab or windowTheracosBio announcedopens in a new tab or window.

As an adjunct to diet and exercise, the oral treatment is indicated for adults with type 2 diabetes, and is not recommended for those with type 1 diabetes or for patients in diabetic ketoacidosis, according to the company.

Of note, the once-daily treatment can also be initiated in patients with stage 3 chronic kidney disease (CKD), a group where metformin is often avoided due to a risk of lactic acidosis.

Underpinning the approval were 23 clinical trials, which tested the agent in over 5,000 adults with type 2 diabetes. Phase III trials showed significant HbA1c and fasting glucose reductions by week 24 as monotherapy, in combination with metformin, or as an add-on to existing regimens containing sulfonylureas, metformin, insulin, and DPP-4 inhibitors. Trials also showed modest improvements in weight loss and systolic blood pressure while on treatment.

Bexagliflozin joins the growing list of SGLT2 inhibitors approved in type 2 diabetes, including empagliflozin (Jardiance), ertugliflozin (Steglatro), canagliflozin (Invokana), and dapagliflozin (Farxiga).

“As a class of drugs, SGLT2 inhibitors have shown tremendous benefit in treating adults with type 2 diabetes,” Mason Freeman, MD, of Massachusetts General Hospital in Boston, said in a statement. “Being involved in all of the clinical trials for Brenzavvy, I am greatly impressed with the efficacy of the drug in reducing blood glucose levels, and I believe it is an important addition to the SGLT2 inhibitor class of drugs.”

In one of the supporting phase III trials involving patients with CKD, the drug elicited 0.31% and 0.43% drops in HbA1c for the stage 3a and stage 3b CKDopens in a new tab or window subgroups, respectively. This 300-participant study also demonstrated significant improvements in body weight, systolic blood pressure, fasting plasma glucose, and albuminuria.

TheracosBio noted a higher incidence of lower-limb amputations compared with placebo in one trial involving type 2 diabetes patients with either established cardiovascular disease (CVD) or those at risk for CVD (8.3 vs 5.1 events per 1,000 patient-years). In total, 23 bexagliflozin-treated patients in the trial underwent amputations — 15 of the toe and midfoot and eight above or below the knee.

Before starting treatment, “consider factors in the patient history that may predispose to the need for amputations, such as a history of prior amputation, peripheral vascular disease, neuropathy and diabetic foot ulcers,” the company stated.

Other safety information included risks for ketoacidosis, volume depletion, urosepsis and pyelonephritis, hypoglycemia with concomitant use with insulin and insulin secretagogues, Fournier’s gangrene, and genital mycotic infections.

Bexagliflozin comes in 20-mg oral tablets, to be taken once daily in the morning with or without food.

CNET’s AI Journalist Appears to Have Committed Extensive Plagiarism


CNET’s AI-written articles aren’t just riddled with errors. They also appear to be substantially plagiarized.

Getty Images

The prominent tech news site CNET‘s attempt to pass off AI-written work keeps getting worse. First, the site was caught quietly publishing the machine learning-generated stories in the first place. Then the AI-generated content was found to be riddled with factual errors. Now, CNET‘s AI also appears to have been a serial plagiarist — of actual humans’ work.

The site initially addressed widespread backlash to the bot-written articles by assuring readers that a human editor was carefully fact-checking them all prior to publication.

Afterward, though, Futurism found that a substantial number of errors had been slipping into the AI’s published work. CNET, a titan of tech journalism that sold for $1.8 billion back in 2008, responded by issuing a formidable correction and slapping a warning on all the bot’s prior work, alerting readers that the posts’ content was under factual review. Days later, its parent company Red Ventures announced in a series of internal meetings that it was temporarily pausing the AI-generated articles at CNET and various other properties including Bankrate, at least until the storm of negative press died down.

Now, a fresh development may make efforts to spin the program back up even more controversial for the embattled newsroom. In addition to those factual errors, a new Futurism investigation found extensive evidence that the CNET AI’s work has demonstrated deep structural and phrasing similarities to articles previously published elsewhere, without giving credit. In other words, it looks like the bot directly plagiarized the work of Red Ventures competitors, as well as human writers at Bankrate and even CNET itself.

Jeff Schatten, a professor at Washington and Lee University who has been examining the rise of AI-enabled misconduct, reviewed numerous examples of the bot’s apparent cribbing that we provided. He found that they “clearly” rose to the level of plagiarism.

We asked Schatten what would happen if a student turned in an essay with a comparable number of similarities to existing documents with no attribution.

“They would be sent to the student-run ethics council and given the repeated nature of the behavior would almost certainly be expelled from the university,” he replied.

The bot’s misbehavior ranges from verbatim copying to moderate edits to significant rephrasings, all without properly crediting the original. In at least some of its articles, it appears that virtually every sentence maps directly onto something previously published elsewhere.

Take this excerpt, for instance, from a recent article by the CNET AI about overdraft protection:

How to avoid overdraft and NSF fees 

Overdraft fees and NSF fees don’t have to be a common consequence. There are a few steps you can take to avoid them.

And compare it to this verbiage from a previously published article in Forbes Advisor, a Red Ventures competitor:

How to Avoid Overdraft and NSF Fees 

Overdraft and NSF fees need not be the norm. There are several tools at your disposal to avoid them.

Sure, the bot’s version altered the capitalization and swapped out a few words for impressively lateral-minded synonyms — “the norm” becomes “a common consequence,” for instance, and “several tools” becomes “a few steps” — along with a few minor changes to the syntax. But apart from those semantic tweaks, the two sentences are nearly identical.

Here’s another excerpt from the same article by CNET‘s AI financial writer:

Sign up for low-balance alerts 

You may be able to receive low balance alerts from your bank’s mobile app, so you know if your account balance is dropping below a certain threshold.

Now compare it to this section from another previously published article, this one from The Balance, another Red Ventures competitor:

Sign Up for Low Balance Alerts 

You can sign up for low-balance alerts through most banks to alert you when your account hits a certain amount.

Again, it seems clear that the AI is simply parsing through and making small modifications to obscure the source.

Sometimes the similarities are almost comical in their lack of subtlety. Take the first sentence of this article, also published by CNET‘s AI:

Gift cards are an easy go-to when buying a present for someone.

And compare it to the first sentence of this previously published Forbes article:

Gift cards are an easy-to-please present for just about anyone.

The kicker on that one? Check out the almost imperceptible difference between those two articles’ headlines. Here’s the CNET AI’s title:

Can You Buy a Gift Card With a Credit Card?

And here’s what Forbes ran with for a headline:

Can You Buy Gift Cards With a Credit Card?

That’s right: the only difference is switching “Gift Cards” to a singular.

Here’s another example, from the same AI-generated CNET article about overdraft fees:

What is overdraft protection?

Overdraft protection is an optional feature offered by banks to prevent the rejection of a charge on a checking account with insufficient funds.

Which, it turns out, appears to be a word salad rephrasing of a line from this article on Investopedia, another Red Ventures competitor.

What Is Overdraft Protection?

Overdraft protection is an optional service that prevents the rejection of charges to a bank account… that are in excess of the available funds in the account.

The AI appears to sometimes also borrow language from writers at CNET‘s sister site Bankrate without giving credit. For example, look at this line from an article published by CNET‘s AI back in November: 

Becoming an authorized user can help you avoid applying for a card on your own, which is a major benefit if you currently have bad credit or no credit history.

And compare it to this wording, previously published by a Bankrate writer:

Becoming an authorized user also lets you avoid having to apply for a card on your own, which is a major benefit if you currently have bad credit or no credit history at all.

All told, a pattern quickly emerges. Essentially, CNET‘s AI seems to approach a topic by examining similar articles that have already been published and ripping sentences out of them. As it goes, it makes adjustments — sometimes minor, sometimes major — to the original sentence’s syntax, word choice, and structure. Sometimes it mashes two sentences together, or breaks one apart, or assembles chunks into new Frankensentences. Then it seems to repeat the process until it’s cooked up an entire article.

A current Red Ventures employee also reviewed examples of the bot’s seemingly lifted work.

“You ever copy your homework off of somebody,” they quipped, “but they told you to kind of rephrase it?”

“It poses the question of what kind of institutions do CNET and Bankrate want to be seen as,” they continued. “They’re just taking these articles and rephrasing a couple of things.”

Are you a current or former Red Ventures employee and want to share your thoughts about the company’s use of AI? Email us at tips@futurism.com. We can keep you anonymous.

In short, a close examination of the work produced by CNET‘s AI makes it seem less like a sophisticated text generator and more like an automated plagiarism machine, casually pumping out pilfered work that would get a human journalist fired.

Perhaps, at the end of the day, none of this should be terribly surprising. At their core, the way that machine learning systems work is that you feed in an immense pile of “training data,” process it with sophisticated algorithms, and end up with a model that can produce similar work on demand.

Investigators have sometimes found examples of AI plagiarizing its own training data. In 2021, for instance, researchers from Johns Hopkins University, New York University and Microsoft found that text-generating AIs “sometimes copy substantially, in some cases duplicating passages over 1,000 words long from the training set.”

As such, the question of exactly how CNET’s disastrous AI was trained may end up taking center stage as the drama continues to unfold. At a CNET company meeting late last week, The Verge reported at the time, the outlet’s executive vice president of content and audience refused to tell staff — many of them acclaimed tech journalists who have written extensively about the rise of machine learning — what data had been used to train the AI.

The legality of using data to train an AI without the consent of the people who created that data is currently being tested by several lawsuits against the makers of prominent image generators, and could become a flashpoint in the commercialization of the tech.

“If a student presented the equivalent of what CNET has produced for an assignment in my class, and if they did not cite their sources, then I would definitely count it as plagiarism,” said Antony Aumann, a philosophy professor at Northern Michigan University who recently made headlines when he discovered that one of his own students had submitted an essay generated using ChatGPT, after reviewing examples of the CNET AI’s similar phrasing to other outlets.

“Now, there is some dispute among academics about exactly what plagiarism is,” he continued. “Some scholars consider it a form of stealing; other scholars regard it as a kind of lying. I think of it in the latter way. Plagiarism involves representing something as your own that is in fact not your own. And that appears to be what CNET is doing.”

CNET did not respond to examples of the bot’s seemingly cribbed writing, nor to questions about this story.

In a sense, the relentless ineptitude of the company’s braindead AI probably obfuscates many of the thornier themes we’re likely to see emerge as the tech continues to spread into the workplace and information ecosystems.

Schatten, for instance, warned that issues around AI and intellectual property are likely to get more ambiguous and difficult to detect as AI systems continue to improve, or even as publishers start to experiment with more advanced systems that already exist (Red Ventures has declined to say what AI it’s using, though the editor-in-chief of CNET has said that it’s not ChatGPT.)

“The CNET example is noteworthy because whatever AI they were using was not drawing from the entirety of the internet and carefully coming up with a new mosaic, but rather just lifting more or less word for word from existing stories,” Schatten said. “But the more sophisticated AIs of today, and certainly the AIs of the future, will do a better job of hiding the origins of the material.”

“And especially once AIs are drawing from the writing of other AIs, which themselves are quoting AI (dark, I know) it might become quite difficult to detect,” he added.

In a practical sense, it seems increasingly obvious that CNET and Red Ventures deployed the AI system and started blasting its articles out to the site’s colossal audience without ever really scrutinizing its output. It wasn’t just that the architects of the program missed obvious factual errors, but that they appear never to have checked whether the system’s work might have been poached.

And to be fair, why would they? As The Verge reported in a fascinating deep dive last week, the company’s primary strategy is to post massive quantities of content, carefully engineered to rank highly in Google, and loaded with lucrative affiliate links.

For Red Ventures, The Verge found, those priorities have transformed the once-venerable CNET into an “AI-powered SEO money machine.”

That might work well for Red Ventures’ bottom line, but the specter of that model oozing outward into the rest of the publishing industry should probably alarm anybody concerned with quality journalism or — especially if you’re a CNET reader these days — trustworthy information.

Cellular Reprogramming Extends Lifespan in Mice, Longevity Startup Says


mouse longevity lifespan Yamanaka factors

Billions of dollars are pouring into longevity startups as a growing body of research shows that aging might not be as inevitable as we assumed. Now, a startup claims to have reached a major milestone by extending the lifespans of healthy mice using a promising approach called cellular reprogramming.

In 2017, scientists at the Salk Institute for Biological Studies in San Diego first showed that it was possible to rejuvenate the cells of mice by resetting their epigenetic markers, chemical modifications to the DNA that don’t alter the underlying genetic code but can regulate the activity of certain genes. These changes have long been suspected of playing a crucial role in the aging process.

The researchers discovered that the approach could increase the lifespan of the mice by as much as 30 percent and significantly rejuvenate some of their tissues, but the experiments were done on animals with the mouse-equivalent of progeria, a disease that causes accelerated aging in humans.

It was unclear whether this kind of life extension would translate to normal healthy mice, but now preliminary results from a longevity startup called Rejuvenate Bio suggest that it does. A non-peer-reviewed paper published to the preprint server bioRxiv claims that the approach can double the remaining lifespan of elderly mice.

“While aging cannot currently be prevented, its impact on life and healthspan can potentially be minimized by interventions that aim to return gene expression networks to optimal function,” Noah Davidsohn, chief scientific officer and co-founder of Rejuvenate Bio, said in a press release. “The study results suggest that partial reprogramming could be a potential treatment in the elderly for reversing age-associated diseases and could extend human lifespan.”

Cellular reprogramming builds on the Nobel Prize-winning work of Shinya Yamanaka, who showed that adult cells could be transformed back into stem cells by exposing them to a specific set of genome-regulating proteins known as transcription factors. The Salk team’s innovation was to reduce the exposure times to the so-called Yamanaka factors, which they found could reverse epigenetic changes to the cells without reverting them to stem cells.

While the approach led to clear increases in lifespan in prematurely aging mice, the fact that no one had been able to replicate the result in healthy mice since then raised doubts about the approach. “Different groups have tried this experiment, and the data have not been positive so far,” Alejandro Ocampo, from the University of Lausanne in Switzerland, who carried out the original Salk experiments, told MIT Technology Review.

But now, Rejuvenate Bio claims that when they exposed healthy mice near the end of their lives to a subset of the Yamanaka factors, they lived for another 18 weeks on average, compared to just 9 weeks for those that didn’t undergo cellular reprogramming.

The mice were already 124 weeks old at the time, so this only represents a 7 percent increase in lifespan. But the company says it’s still a significant demonstration of the potential life-extending powers of cellular reprogramming, and the treated mice also showed improvements in a range of health metrics.

Another reason why the research is interesting, though, is the method by which the Yamanaka factors were administered. Previous studies have generally relied on genetically modifying mice to produce the factors themselves, but this study delivered them to the animals’ cells using repurposed viruses, which is the approach used in clinically approved gene therapies.

The results have yet to be peer reviewed, so should be taken with a pinch of salt until other groups are able to replicate them, but there is growing evidence of the potential therapeutic benefits of cellular reprogramming. Recent research on mice has shown that it can boost liver regeneration and help restore sight in animals with glaucoma.

It’s likely to be a long road to human trials, as there are significant question marks about potential side effects, including concerns that the approach could increase the risk of cancer. But promisingly, recent research on mice from the Salk team has shown that long-term treatment with Yamanaka factors led to significant rejuvenating effects on the animals’ tissues without causing any cancers. The research also found that the longer the treatment time, the better the results.

Further work will need to be done to validate the research from Rejuvenate Bio, but the results suggest that age-reversing treatments may soon be within reach.

DARPA Wants to Develop a Drug to Make People Resistant to Extreme Cold


trees with snow cold person walking

From painkillers to antihistamines to caffeine and beyond, we’ve found many ways to get our bodies to tolerate uncomfortable circumstances, for better and for worse. Now DARPA wants to add another to the list: getting the human body to better tolerate extreme cold.

The idea doesn’t sound like a great one at first glance; our bodies aren’t made to live in the cold, nor even withstand it for more than a little while. Our teeth start to chatter, we shiver, and eventually lose feeling in extremities, all signals that we need to get ourselves warm, stat—otherwise we can get hypothermia, frostbite, or worse.

The Defense Advanced Research Projects Agency (DARPA) has a few different motives for this research, but the primary one shouldn’t be surprising (though it’s still a bit creepy, in my opinion): enabling soldiers to be comfortable in cold places for long periods of time. The technology, if successful, could also be used to help explorers or adventurers (at high altitudes where it’s cold or in places like Alaska or the Arctic, for example) better tolerate cold, or to treat hypothermia patients.

Last week, Rice University in Houston announced that one of its assistant professors of bioengineering, Jerzy Szablowski, received a Young Faculty Award from DARPA to research non-genetic drugs that can “temporarily enhance the human body’s resilience to extreme cold exposure.”

Thermogenesis is the use of energy to create heat, and our bodies have two different ways of doing this. One is shivering, which we’re all familiar with. The other, which Szablowski simply calls non-shivering thermogenesis, involves burning off brown adipose tissue (BAT), or brown fat.

This type of fat exists specifically to warm us up when we get cold; it stores energy and only activates in cold temperatures. Most of our body fat is white fat. It builds up when we ingest more calories than we burn and stores those calories for when we don’t get enough energy from food. An unfortunate majority of American adults have the opposite problem: too much white fat, which increases the risk of conditions like heart disease and Type 2 diabetes.

While white fat is made of fatty acids called lipids, brown fat is dense in mitochondria (the component of cells where energy production occurs). When we get cold our bodies start pumping out the hormone norepinephrine, which attaches to receptors on brown fat cells, signaling the mitochondria to create energy—and warming us up in the process.

Szablowski will be trying to find ways to boost the BAT response. “If you have a drug that makes brown fat more active, then instead of having to spend weeks and weeks adapting to cold, you can perform better within hours,” he said. He added that his research will focus on finding a site to intervene in the BAT response, “like a protein or a process in the cell that you can target with a drug.”

Is it possible to change the body’s normal BAT response without needing to burn through more brown fat, which healthy adults don’t have a ton of to spare? We’ll see. Though white fat and brown fat have different compositions, it’s possible that Szablowski’s research could lead to new ways to eliminate white fat and treat obesity as well.